Un coup de chaud… -...

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  • Un coup de chaud Rendez-vous de lurgence 22 mai 2014 Yannick RABOUL SAMU 67 DESC mdecine durgence

  • Cas clinique Homme 21 ans

    Sans antcdents

    10 km de Strasbourg 18 mai 2014

    Temprature 20c, humidit 40%,

    vent 7 km/h

    Dpart 11h15

  • Histoire de la maladie En fin de course appel SAMU 12h26 Crise convulsive, Inconscient

    Bilan SAMU larrive Coma aractif, glasgow 3 CTCG FC 170 bpm, TA 95/54 Tc 39,5

    IOT en squence rapide, SSI froid

  • En ranimation Exam CV: tachycarde, le reste sp

    TA 90/50 mmHg

    Mouvements en flexion des mb infrieurs la manuvre de PMF

    Abdomen souple dpressible

    Vomissements itratifs

    Dbcle diarrhique

  • ECG

  • Biologie dadmission Cratinine 175 mol/L, ure 8,4 mmol/L

    K+ 6,28 mol/L

    CPK 1.500 U/L

    TGO 2 x N

    TP 70%, Fg 1,82 g/L

    pH 7,21, Bicar 18,5 mM, Lactate 2,9 mM

    NFS sp

  • ETT Altration globale FEVG 30-35%

    Pas datteinte du cur D

    Pressions de remplissages non leves

  • Evolution 24h Majoration Insuffisance rnale

    (230 mol/L, Ure 12 mmol/L)

    Majoration Rhabdomyolyse 15.000 U/L

    Pic Troponine 2,22 g/L

    CIVD (TP 19%, Fg 0,7g/L, D-dimres > 20.000 g/L)

    Thrombopnie 46.000/mm3

    Cytolyse hpatique (TGO 700 U/L, TGP 400 U/L)


  • Evolution 72h

    Dbut de rgression insuffisance rnale sans EER

    Majoration cytolyse (TGO 3500 U/L, TGP 4200 U/L)

    Hyper-bilirubinmie 111 mol/L

    Persistance CIVD et thrombopnie

    Rcupration dune FEVG normale sans amines

  • Ce jour Toujours en ranimation

    Cratinine 157 mol/L, Ure 8 mmol/L sans EER

    Fonction hpatique: Bilirubine 152 mol/L TGO 3500 U/L () TGP 7300 U/L ()

    TP 42%, Facteur V 51%

    D-dimres 6020 g/L, Fg 2,68 g/L

  • Au total Atteinte neurologique

    Atteinte digestive

    Atteinte hmodynamique

    Insuffisance rnale aigue sans EER Fonctionnelle et organique

    Insuffisance hpato-cellulaire, cytolyse


    Antibiothrapie, prlvements striles

  • Hyperthermies deffort

  • Hyperthermie et fivre Hyperthermie Thermostat central reste rgl 37c Mcanismes de thermolyse

    - Lsion hypothalamus ? (inhibe thermolyse)

    - Dfaillance cardio-vasculaire ?

    Fivre Action des pyrognes circulants (TNFet IL-1) Thermostat augment Mcanismes de thermognse

  • Hyperthermies Coup de chaleur classique (exogne)

    Hyperthermie deffort (endogne) +/-Majore par conditions extrieures

    Intoxication (cocane, ecstasy)

    Hyperthermie per-anesthsique

    Dsquilibre production vacuation

    Cause exogne => Alerte sanitaire ?

  • Vague de chaleur ?

    France 30c

    US 32,2c

    Grande-Bretagne +4c par rapport la moyenne

    Paroxysme thermique entrainant une surmortalit

  • Rgulation Rgion pr-optique de lhypothalamus antrieur

    Thermo-rcepteurs cutans et musculaires

    Consquences: Vasodilatation cutane intense Dbit cutan au dpens du rseau splanchnique Sudation Diminution production de chaleur

  • Thermorgulation Production de chaleur endogne 50 W

    => jusque 500 W en cas deffort physique

    Pertes de chaleur

  • Sudation Principal facteur de thermolyse leffort 1,7 ml de sueur = 1 Kcal de chaleur vacue Adulte europen: Dbit sudoral max 1,5 L/h (perte eau et sel +++)

    Efficacit module par Hygromtrie leve > 60% Absence de vent Vtements impermables

  • Adaptation Tolrance thermique Heures jours (sudation, hyperventilation)

    Acclimatation Plus de 7 jours Augmentation volume plasmatique Modulation du SRAA (diminue pertes de sel) Rle des HSP: inhibent cytokines pro-inflammatoires

  • Stress thermique Lsions cellulaires, dnaturation protines

    SRIS +/- SDMV

    Immunodpression / infections secondaires

    Libration NO, micro-thrombi, CIVD

    Phnomnes pas toujours rversibles malgr correction temprature

    Parallle avec les tats de choc (septique ++)

  • Coup de chaleur =

    Hyperthermie souvent > 40c

    => Valeur pronostique

    Atteinte neurologique Confusion, inconscience, convulsion, coma Syndrome pyramidal, crbelleux, mning Installation insidieuse (heures, jours)

  • Facteurs de risque individuels Capacit de lindividu se soustraire de la chaleur OH, dpendance, pathologie psychiatrique Architecture (baies vitres) Accs la climatisation (hpital) Vie citadine

    Dysfonction de lvacuation thermique (ge) Vieillissement CV, cardiotropes Capacit sudorale

    Polymorphisme des HSP

  • Clinique Tguments Chaleur cutane, dilatation veineuse, rash ptchial Anhydrose, langue rtie

    Cardio-vasculaire Tachycardie > 150 bpm HypoTA, collapsus

    Abdominal Nauses, vomissements, diarrhe, ictre

    Dshydratation globale

  • Para-clinique Hyperleucocytose PNN, Thrombopnie

    Coagulopathie, CIVD

    Insuffisance hpato-cellulaire (greffe)

    Profil hyperkintique initialement

    Insuffisance cardiaque secondaire

    avec hypokinsie globale

  • Para-clinique Hyponatrmie

    (hyperhydratation orale hypotonique)

    Insuffisance rnale fonctionnelle puis organique

    Hyperkalimie secondaire la rhabdomyolyse

    Acidose mtabolique, hyper-lactatmie +/- compense par lhyperventilation

    Anomalies ECG non spcifiques

  • Hyperthermie - inflammation Hyperactivation leucocytaire par rapport au sepsis

    Etat pro-inflammatoire major

    Mais HSP suractives

    Hypofibrinognmie > sepsis

  • except IL-18, purchased from MBL, Naka-kuNagoya, Japan), according to the manufactur-ers instructions. IL-8 was also assayed in PMNand monocyte culture supernatants. The de-tection limits were 5 pg/mL except for IL-1RA(18 pg/mL) and IL-18 (12 pg/mL).

    The following proteins were assayed in du-plicate in plasma with specific ELISAs: heatshock proteins (HSP) 60 and 70 (Stressgen,Victoria, Canada, respective detection limits3.0 and 0.5 ng/mL), complement C5a (BD op-tiEIA, San Diego CA, detection limit 60 pg/mL), soluble thrombomodulin (Serbio, Gen-nevilliers, France, detection limit 20 ng/mL).

    Quantification of Reactive Oxygen SpeciesProduction. Reactive oxygen species (ROS)were quantified in duplicate by using a chemi-luminescence kit in whole blood, according tothe manufacturers instructions (ABEL,Knight Scientific, Plymouth, UK). Briefly,whole blood was incubated with the photo-protein pholasine and stimulated with phorbolmyristate acetate (Sigma); light emission wasthen measured with a chemiluminometer (Au-toLumat, Berthold Technologies GmbH, BadWildbad, Germany).

    Plasma Matrix Metalloproteinase-2 and -9Assays. Pro- and active-matrix metalloprotein-ase (MMP)-2 and -9 were measured in dupli-cate in 0.5 !L of citrated plasma by means ofgelatin zymography and densitometric analy-sis of the substrate lysis zone (20). Results (inmUDO/mL) were expressed as a percentage ofnormal (value in pooled plasma of 20 healthycontrols).

    Statistical Analysis. Results were ex-pressed as median (range). For continuousvariables, groups were compared with theMann-Whitney U test (two groups) or withKruskal-Wallis (three groups). The Chi-squaretest or Fishers exact test were used for qual-itative variables. Bivariate correlations be-

    tween parameters were calculated with theSpearman rank correlation test. The p values"0.05 were considered statistically signifi-cant. As this study is mainly exploratory, nocorrection for multiple testing was used.


    Clinical Observations

    The clinical characteristics of the pa-tients (heatstroke and sepsis) are indi-cated in Table 1. All heatstroke patientsbut one suffered at least one underlyingdisease or were having chronic medica-tion. Seven patients were found to havepsychiatric medication (namely phe-nothiazine, lithium, and selective seroto-nin reuptake inhibitors). Eight patientswere treated for chronic arterial hyper-tension (2 were treated with diuretics andthe other with beta-blockers or with an-giotensin-converting enzymes inhibi-tors). Finally, 3 patients suffered fromchronic respiratory disease. Fifteen pa-tients had shock, since hepatic or renaldysfunction were present in 4 and 17patients, respectively. Core temperaturesranged from 38C to 41C at the time ofblood sampling. In-hospital mortalityrate was 78% (14 of 18), 7 patients dyingfrom multi-organ failure during the firstweek and 7 dying from neurologic disor-ders during ICU stay.

    Among the 14 patients with severesepsis, 5 had postsurgical peritonitis, 7had pneumonia and 2 had uro-sepsis.Preexisting comorbid diseases were

    present in all but 1 (hypertension, 7; di-abetes, 2; obesity, 1; atrial fibrillation, 3;chronic obstructive lung disease, 3; epi-lepsy, 2).

    No significant differences were foundbetween patients with heatstroke and se-vere sepsis with regard to SimplifiedAcute Physiology Score II at admission,the use of mechanical ventilation and/orvasoactive drugs, presence of renal failureand PaO2/FIO2 ratio. However, heatstrokepatients were more often males, hadhigher SOFA score, lower Glasgow ComaScale score and higher central core tem-perature compared with severe sepsis pa-tients. In addition, cardiac troponin, bil-irubin, and arterial lactate were allsignificantly higher in heatstroke pa-tients. The overall in-hospital mortalitywas 78% in the latter compared with only14% in patients with severe sepsis.

    The healthy control group involved 9men and 9 women free from any medica-tion; the median age (67 yrs [range 3382]) was similar to that of the two patientgroups.

    Circulating Levels of Mediators

    Plasma levels of IL-6 were signifi-cantly increased in both patient groups,with significant higher concentrations inseptic patients as compared with heat-stroke patients (Table 2). The levels oftumor necrosis factor-# were slightly butsignificantly increased in both patientgroups, the higher levels being observedduring severe sepsis. IL-1$ was undetect-able in both patient groups. The levels ofIL-18 were significantly increased onlyduring severe sepsis. IL-8 and C5a plasmalevels were significantly increased in bothpatient groups, with higher IL-8 levels inheatstroke patients as compared with se-vere sepsis (Table 2). A positive correla-tion was found between plasma IL-6 and-8 levels in heatstroke patients (r % .91,p " 0.0001).

    Interestingly, this proinflammatorystate was offset by regulatory mecha-nisms, as reflected by a similar significantincrease in IL-1RA plasma levels in theheatstroke and septic patients as com-pared with the healthy controls (Table 2).HSP60 and 70 plasma levels were alsosignificantly enhanced during heatstroke;both proteins were increased in only 5patients with severe sepsis.

    As shown in Table 2, pro-MMP-9 levelswere strongly increased in heatstroke pa-tients in whom it could be studied (lastassay of the study) as compared with sep-

    Table 1. Clinical and biological characteristics of heatstroke and severe sepsis patients at intensivecare unit admission

    Heatstroke Patients(n % 18)

    Severe Sepsis Patients(n % 14) p

    Age (yr) 68 (3383) 69 (3383) 0.61Male, n (%) 9 (50) 12 (85) 0.07SAPS II 65 (2590) 60 (2470) 0.25SOFA 13 (319) 10 (213) 0.0066Glasgow coma score 4 (315) 13 (615) 0.015Maximal core temperature (C) 41.4 (39.142.4) 38.5 (3639.5) "0.0001Time to achieve (t " 385) 5.5 (223) Mechanical ventilation, n (%) 15 (83) 12 (85) 0.84PaO2/FiO2 (mm Hg) 131 (61222) 126 (106160) 0.35MAP (mm Hg) 65 (5080) 57.5 (4075) 0.06Vasoactive drugs, n (%) 15 (83) 11 (78) 0.65Cardiac troponin I (!g/L) 10.3 (0.2313) 0.4 (0.213) "0.0001Creatinine (!mol/L) 180 (83303) 146.5 (31450) 0.74Bilirubin (!mol/L) 19 (954) 10.5 (627) 0.0075Arterial lactate (mmol/L) 4.5 (1.39.4) 1.9 (18.2) 0.0014In-hospital mortality, n (%) 14 (78) 2 (14) 0.049

    The results are indicated as median (range) or number of patients (%) when indicated.SAPS, Simplified Acute Physiology Score; SOFA, Sepsis-Related Organ Failure Assessment; MAP,

    mean arterial pressure.

    2290 Crit Care Med 2008 Vol. 36, No. 8

  • Prise en charge

  • URGENCE THERAPEUTIQUE Soustraction ambiance chaude

    Correction des dtresses vitales

    Rfrigration QSP temp < 39,4 c RAPIDEMENT +++ Par tous moyens disponibles Milieu non climatis = FDR pjoratif Pas deffet des TTT anti-pyrtiques ni dantrolne

    Hydratation, remplissage

  • Plan de secours Indicateurs Patients > 70ans, patients fbriles, SAU, dcs

    PACE (plan daction chaleur extrme) Glace Rquisition ventilateurs, climatiseurs Redfinition moyens SMUR Rquisition SSPI

    Mdecine de catastrophe

  • Plan de prvention Alerte mtorologique prcoce

    Reprage des personnes isoles

    Ouverture de milieux climatiss (cinma)

    Au moins un endroit climatis

    Surveillance, dpistage tolrance clinique

    Adaptation thrapeutique (diurtiques)

  • Rfrences Hyperthermie de ladulte et coup de chaleur P. Hausfater et B. Riou EMC

    Leukocyte activation: the link between inflammation and coagulation during heatstroke. A sudy of patients during the 2003 heat wave in Paris Huisse et al. CCM 2008

  • Merci . . .